Occurrence: Worldwide. Species affected: All. Age affected: All.

Cause: Consumption of feed containing grains infected with fungi of the genus Fusarium, containing tricothecene toxins.

Effects: Symptoms depend on dose of toxin, age of bird and duration of exposure. Signs include feed refusal, impaired growth, uneven and poorly formed feathers and emesis (vomiting). Thin-shelled eggs, reduced egg production, facial swelling, caustic injury to skin, cyanotic (blue coloured) combs and wattles, seizures and tremors may also be seen.

Mycotoxins are toxic metabolic byproducts of fungal growth on grains. High moisture content of grains can lead to fungal growth and toxin production. Fungi can produce toxins before or after grain harvest. Drought and insect damage to grain increase susceptibility of grain to fungal growth.

Disease is acute to chronic depending on dosage of toxin (higher-acute), age of bird (young birds have acute, older have chronic), and duration of exposure (longer periods cause chronic toxicosis).

Consumption of feed containing grains infected with fungi producing trichothecenes toxins cause the disease. The following trichothecenes: T-2, diacetoxyscirphenol (DAS) and deoxynivalenal (DON or vomitoxin) can be produced by Fusarium trichinctum, F. calonectria, F. gibberella, F. cephalosporium and F. trichoderma.

Feed contaminated with trichothecenes containing toxin which are very caustic. It can occur in corn, sorghum, barley, safflower seed, oats and brewers grain.

Signs include feed refusal, impaired growth, uneven and poorly formed feathers, and emesis (vomiting).

Thin shelled eggs, reduced egg production, swelling of the face, caustic injury to skin, cyanotic (blue-coloured) combs and wattles, seizures and tremors may be seen.

Whitish to yellow, focal nodules in based of mouth, near the salivary ducts and tongue can occur. An inflamed GI tract, atrophy of bursa and thymus, necrosis of gizzard and proventriculus, dermatitis on the toes, pale or yellow bone marrow, yellow haemorrhagic liver and gout can also be seen.

Feed analysis for toxins and feed refusal in many farm animals are diagnostic. It simulates wet pox, vitamin A deficiency, thrush, trichomoniasis, ochratoxicosis and aflatoxicosis, IBD and visceral gout.

Feed low moisture corn (below 14%). Do not add mouldy corn to the finished feed. Mouldy feed can be prevented with a mould inhibitor such as proprionic acid. Even so, quality control of feed is necessary. Grains should be checked for B1 (corn with greater than 16% moisture).

Contaminated feed can be diluted with noncontaminated grain or treated with ammonia, which inactivates the toxin. However, local regulations are sometimes prohibitive of these practices.

Contaminated feed can be fed to older pullets, which are less susceptible.

Two feed bins at the farm will reduce grain and feed storage time, which reduces fungal growth and toxin formation.

Aluminosilicates in the feed such as zeolites will bind and inactive aflatoxin. Other binding agents such as those based on glucomannans can be used. Pelleting can kill fungus, but will not always inactivate toxins.

Gentian violet* kills fungi and binds aflatoxin.

Increasing the protein content of feed by 1%, increasing vitamin and mineral content of feed and adding Gentian violet to feed have a sparing effect on aflatoxin induced disease.

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